Abstract

Introduction: Hepatitis Delta Virus (HDV) infects those that are already infected with the Hepatitis B Virus (HBV), resulting in a serious infection that may damage hepatocytes. We present a patient that undergoes interferon therapy for chronic hepatitis delta infection with an emphasis on efficacy and side effects of treatment. Case Description/Methods: A 20 year old previously healthy African male presents with progressive fatigue. Bloodwork demonstrates elevated liver enzymes, thrombocytopenia, positive Hepatitis B surface antigen and core antibody, and is negative for hepatitis B e-antigen. HBV DNA levels are 30 IU/mL (reference range < 10 IU/mL). Six months later, liver enzymes remain elevated (AST 100 U/L, ALT 186 U/L). Liver biopsy confirms chronic hepatitis and moderate fibrosis with Metavir grade A3, stage F2, and is consistent with viral hepatitis infection. The biopsy also reveals schistosomiasis of the liver, for which the patient is treated with two series of Praziquantel 1800 mg, 3 times per day. Schistosomiasis resolve following treatment, yet liver enzymes remain elevated. Subsequent bloodwork is positive for HDV, with very high levels of HDV RNA at 14,000,000 IU/mL. The patient is started on tenofovir 300mg/day and peginterferon 180 mcg/week. This therapy is maintained for over 4 years, with side effects of headache and fatigue. Liver biopsy near end of treatment reveals mild portal inflammatory infiltrate composed predominantly of lymphocytes with scattered foci of lobular inflammation; Metavir grade 1, stage 0. Bloodwork at this time shows improvement in liver enzymes with AST 57 U/L and ALT 39 U/L. Patient stopped interferon due to side effects after four years of suppressive treatment. The most recent bloodwork shows HBV and HDV viral suppression via PCR, and negative Hepatitis B surface antigen. Liver surveillance via ultrasound reveals no evidence hepatocellular carcinoma during the duration of therapy. Discussion: Hepatitis delta virus (HDV) is a blood-borne virus that infects human hepatocytes. The replication of HDV depends upon a simultaneous infection with the Hepatitis B virus (HBV). Chronic HDV infections manifest as a rapidly progressing form of viral hepatitis, and can lead to cirrhosis with an increased risk of hepatocellular carcinoma. Currently, HDV has no approved treatment options from the United States Food and Drug Administration, and the only option for treatment is pegylated interferon-alpha.

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